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Compartment Syndrome

Compartment syndrome, if not identified and acted upon early, will result in irreversible damage to neuromuscular soft tissue. Therefore, the healthcare professional must be aware of the risks, signs and symptoms, unusual circumstances, and appropriate interventions with this syndrome. Compartment syndrome is a life-threatening condition in which increased tissue pressure in a confined anatomical space causes decreased blood flow leading to ischemia and dysfunction of contained myoneural elements. It is marked by pain, muscle weakness, sensory loss, and palpable tenseness in the involved compartment. Ischemia can lead to necrosis resulting in permanent impairment of function. Increased pressure within the compartment results from bleeding and swelling into the closed space which in turn causes pressure on the vital structures. There is elevation of interstitial pressure in a closed fascial compartment that results in microvascular compromise. As the duration and magnitude of interstitial pressure increases, myoneural function is impaired and necrosis of soft tissues eventually develops. Compartment syndrome can occur where there is significant edema in a compartment within the hand, forearm, upper arm, buttock, legs, feet, and occasionally the abdomen. Usually compartment syndrome occurs due to fractures of the tibia or forearm, in vascular injuries, or burns. Almost any injury or surgery can cause the condition.

Physiology

Arteries and their subdivisions bring freshly oxygenated blood to the tissues, and the associated venous system returns deoxygenated blood to the venous circulation. The human body has a number of areas that function as closed compartments to this delivery system. There are three main compartments in the forearm and four main compartments in the lower leg. The long bones of the limbs, for example, are joined and surrounded by sheets of tough and relatively inelastic tissue called fascia which create comparatively inflexible boundaries. The placement of the fascia is such as to divide the leg, for instances, into a number of sections or compartment. These compartments contain muscles, arteries, veins, and nerves. These compartments generally have a fairly constant volume that permits only slight variation. If swelling occurs in these compartments the subsequent rise in compartment pressure can cause serious damage.

The arterial blood system continues to bring blood into the compartment, but low pressure veins and their subdivision have a low intra-luminal pressure that is restricted. When this occurs it is further compounded by the release of fluid from the blood vessels resulting in a further rise in compartment pressure that perpetuates the cycle. Edema within the closed compartment will increase the pressure within that compartment eventually compromising the vascular supply. Such compromise will lead to further ischemia and edema formation. A vicious cycle will be established as cells become deprived of oxygen.

Subsequent necrosis of muscle and loss of capillary wall integrity will lead to transudation, exudation, and the development of massive edema within the compartment. Rhabdomyolysis then occurs. Rhabdomyolysis is the dissolution or breakdown, of striated muscle that results in the production of myoglobin. Myoglobin is known to cause acute renal failure. If untreated, rhabdomyolysis may lead to myoglobinuria, permanent

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neurovascular damage, renal failure, sepsis, and even death. This occurs as the myoglobin is released into the circulation where it can occlude the distal convoluted tubule and precipitate renal failure.

Significant fluid loss into damaged tissues leads to hypovolemia and metabolic acidosis. This not only acts as a potent pre-renal cause for renal impairment but also enhances the nephritic effect of myoglobin. Severe metabolic complications may present after reperfusion when the damaged membranes continue to leak, aggravating edema formation and increasing the pressure in the closed osteofascial compartment. Rhabdomyolysis is well documented as a secondary cause in a range of conditions related to skeletal muscle injury.

The syndrome may develop as quickly as within the first 30 minutes to 1-2 hours post trauma. Or it may develop postoperatively, post fracture reduction, or in as late as 5-6 days. If it is allowed to last for more than 6 hours, neuromuscular damage becomes irreversible. Splinting, traction, early closed reduction with casting, or early surgery for fractures reduce the risk of Compartment Syndrome.

There are three categories of etiology:

1. Decreased compartment size can be caused by restrictive dressings, splints or casts, excessive traction, or premature closure of fascia.

2. Increased compartment content can be caused by a fracture that causes bleeding or from

a vascular injury, burns, infiltrated IV infusion, swollen or inflamed bowel, or snakebites. The first response is to elevate the extremity. However, when the extremity is elevated too high above heart level, this compromises arterial perfusion, which further compounds the ischemic problem.

3. Externally applied C can be caused from restrictive dressings, prolonged compression

from lying on a limb or crushing injuries of soft tissue.

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Compartment Syndrome Pathophysiology

Insult/Injury

Vascular C (Microvascular and Venous Congestion)

Hypoxia

Cell Death and Protein Release

Edema

Increased Intra-compartmental Pressure

Further Cell Damage

C Necrosis

Death Amputation Permanent Disability

Signs and Symptoms

Compartment syndrome usually presents after reperfusion of a limb. Pain and swelling may not occur immediately. The first signs usually occur after the patient has regained consciousness, undergone their post-anesthetic care, and returned to the unit. Often several hours are reported as uneventful before the first signs and symptoms are reported. The first suspicions are usually aroused when a patient complains of severe pain in the lower legs when they have recovered consciousness or a few hours after surgery. Some patients may even describe pain despite postoperative epidural anesthesia. The patient’s leg may appear tense and swollen. The level of pathological pain is found to be far greater than the ordinary postoperative pain to be expected from the surgical intervention.

The diagnosis of compartment syndrome requires a high index of clinical suspicion. Timing of identification and intervention with compartment syndrome is crucial to a positive patient outcome. It is possible that an initial diagnosis of deep vein thrombosis (DVT) may interfere with the correct diagnosis. The measurement of compartment pressures will confirm the suspicions of compartment syndrome while venous Doppler studies will confirm a DVT. Remember the “6 P’s” of compartment syndrome:

1. Paresthesia Subtle first symptom

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Best elicited by direct stimulation

Complaints of tingling or burning sensations

Loss of 2 point discrimination

Can lead to numbness

2. Pain Out of proportion to the injury

Elicited by passive stretching of the involved compartment

Described as throbbing or deep – localized or diffuse

Increases with the elevation of the extremity

Unrelieved by narcotics

May not be present if central or peripheral sensory deficits are also present

3. Pressure Involved compartment or limb will feel tense and warm on palpation

Skin is tight and shiny

Skin may appear cellulitic

Direct compartment pressure of 30-40 mmHg as measured by a wick, continuous infusion, or

injection method such as the Stryker monitor – normal intracompartmental tissue pressure is 0-10 mmHg.

Differential pressure of greater than 30 mmHg – diastolic blood pressure minus compartment

pressure – as long as diastolic pressure remains high enough or at least 30 mmHg, the compartment will be perfused and there may not be a need for surgical decompression.

Whiteside’s theory suggested that the development of compartment syndrome depends not

only on intra-compartmental pressure but also depends on systemic blood pressure – diastolic pressure minus compartment pressure should be > 30 mmHg.

Example 1:

80 = patient diastolic B/P

-20 = direct compartment pressure

60 = differential pressure (adequate compartment perfusion)

Example 2:

80 = patient diastolic B/P

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-60 = direct compartment pressure

20 = differential pressure (adequate compartment perfusion)

4. Pallor Late sign

Pale, grayish or whitish tone to skin

Prolonged capillary refill (>3 seconds)

Cool feel to skin upon palpation due to lack of capillary perfusion

5. Paralysis Late sign

May start as weakness in active movement of involved or distal joints

Leads to inability to move joint or digits actively

No response to direct neural stimulation due to damage

6. Pulselessness Late sign

Very weak or lack of palpable or Doppler audible pulse

Due to lack of arterial perfusion

Other warning signs of Compartment Syndrome:

1. Fractured blisters: represent areas of necrosis of the epidermis and separation of the skin layers. Occur as the body attempts to relieve the pressure in the compartment.

2. Laboratory findings: elevated WBC (white blood cell count) and ESR (erythrocyte sedimentation

rate) levels due to the severe inflammatory response 3. Elevated temperature due to ischemia/necrosis of tissue and possible infectious response. 4. Elevated Serum Potassium due to cell damage. 5. Lowered Serum pH levels due to acidosis 6. Stretch pain or pain on passive extension or hyperextension of digits (toes or fingers, depending

on the site)

Don’t lose valuable time waiting for laboratory findings. Be vigilant to assessment of the “6 P’s”

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Treatment

When compartment syndrome is diagnosed and treated early, full recovery usually follows. When initial signs and symptoms appear, loosen any external constrictive dressings or cut the cast. Other measures are to position the extremity at the level of the heart not above the heart and provide adequate hydration of the patient to maintain arterial blood pressure. Accurately monitor compartment pressures.

Medical decompression may be instigated if compartment syndrome is suspected and intra-compartment pressures are only marginally increased. A mannitol infusion has been reported as effecting a complete resolution.

Fasciotomy, or surgical decompression, is a surgical incision of the affected compartments. It may be required if conservative interventions are not effective in interrupting the edema-ischemia cycle. As soon as the fascia is sectioned, or surgically split open by an incision through all layers down to and including the fascia, the compartmental contents can bulge, thus allowing pressures to decline along with reinstitution of the normal circulatory pattern.

If performed Fasciotomy should be done in less than 6 hours and no later than 12 hours after onset of symptoms. If the procedure is performed during this time frame it is likely to prevent myoneural deficits. Fasciotomy must be undertaken by a skilled surgeon, ensuring that all compartments (for instance all four in the lower leg) are accessed through a single lateral incision or double vertical whenever possible.

During fasciotomy it is vital to identify and protect nerves. Wounds are usually left open protected by suitable sterile dressings. Inspection of the wound after 48 hours may necessitate further necrotic tissue excision. Delayed skin closure or skin grafting may become treatment options. Adequate analgesia and antibiotic coverage are essential for improving outcomes.

In cases where treatment and prophylaxis of renal failure associated with rhabdomyolysis is suspected or diagnosed, prompt fluid and metabolic correction is essential to re-establish a good urine output. Mannitol has also been beneficial as a renal vasodilator and intravascular expander and aids to induce osmotic diruesis. If these methods fail dialysis may be necessary.

Source: http://www.ceufast.com/courses/176/176.htm

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